Immunohistochemical demonstration of choline acetyltransferase of a peripheral type (pChAT) in the enteric nervous system of rats

Nakajima, Kyoji; Tooyama, Ikuo; Yasuhara, Osamu; Aimi, Yoshinari; Kimura, Hiroshi

doi:10.1016/s0891-0618(99)00058-7

Cited by 72 publications

(74 citation statements)

References 34 publications

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“…Since NGF was not examined in this study, we cannot determine whether increased neuronal sprouting was involved in maintaining the observed increase in ChAT. Recent publications have found a splice variant of ChAT called pChAT, which has been shown to be exclusively localized to neuronal cells and fibers in intramural ganglia (23) and submucosal ganglia (6,39). Few publications exist characterizing this protein, and a commercially available antibody is not yet available.…”

Section: Discussionmentioning

confidence: 99%

Neonatal maternal separation of rat pups results in abnormal cholinergic regulation of epithelial permeability

Gareau

Jury

Perdue

2007

American Journal of Physiology-Gastrointestinal and Liver Physi

128

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Gareau MG, Jury J, Perdue MH. Neonatal maternal separation of rat pups results in abnormal cholinergic regulation of epithelial permeability. Am J Physiol Gastrointest Liver Physiol 293: G198-G203, 2007. First published May 17, 2007; doi:10.1152/ajpgi.00392.2006.-Neonatal maternal separation (MS) predisposes adult rats to develop stressinduced mucosal barrier dysfunction/visceral hypersensitivity and rat pups to develop colonic epithelial dysfunction. Our aim was to examine if enhanced epithelial permeability in such pups resulted from abnormal regulation by enteric nerves. Pups were separated from the dam for 3 h/day (days 4 -20); nonseparated (NS) pups served as controls. On day 20, colonic tissues were removed and mounted in Ussing chambers. Horseradish peroxidase (HRP) flux was used to measure macromolecular permeability. HRP flux was increased in MS versus NS pups. The enhanced flux was inhibited by the cholinergic muscarinic antagonist atropine and the nicotinic antagonist hexamethonium. The cholinergic component was greater in tissues from MS versus NS pups, suggesting that increased cholinergic activity was responsible for the MS elevated permeability. Western blots and immunohistochemistry of colonic tissues demonstrated increased expression of choline acetyltransferase (ChAT) in MS pups, indicating greater synthesis of acetylcholine. Since a previous study indicated that corticotrophin-releasing factor (CRF) mediates barrier dysfunction in MS pups, we examined if the two pathways were linked. In MS tissues, nonselective CRF receptor antagonism inhibited the enhanced flux, and the addition of atropine did not produce further inhibition. Using selective receptor antagonists, we identified that CRF receptor 2 was involved in mediating this effect. These findings suggest that CRF, via CRF receptor 2, acts on cholinergic nerves to induce epithelial barrier dysfunction. Our study provides evidence that MS stimulates synthesis of acetylcholine, which, together with released CRF, creates a condition conducive to the development of epithelial barrier defects. stress; colonic; barrier THE NEONATAL PERIOD is an important developmental period in humans and rodents, and stress during this time can have long-lasting effects on behavior and physiology. Maternal separation (MS) is a well-characterized model of early life stress used in the study of anxiety and depression (17, 31) as well as intestinal dysfunction (1,2,7,28,37). The physiological response to stress is controlled by the hypothalamicpituitary adrenal (HPA) axis, which develops during the neonatal period. Exposure to stress during this time results in the formation of a dysregulated axis with a compromised ability to downregulate the synthesis of corticotrophin-releasing factor (CRF), a key stress hormone (26).Adult rats of a stress susceptible strain that are subjected to daily separation from the dam during the neonatal period demonstrate increased colonic permeability (2) and visceral hyperalgesia (28). Adult rats that are not genetically susceptible t...

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Section: Discussionmentioning

confidence: 99%

Neonatal maternal separation of rat pups results in abnormal cholinergic regulation of epithelial permeability

Gareau

Jury

Perdue

2007

American Journal of Physiology-Gastrointestinal and Liver Physi

128

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Section: Discussionmentioning

confidence: 99%

“…ChAT, the enzyme synthesizing acetylcholine, is contained in ϳ60% of rat myenteric neurons (41). However, ChAT immunoreactivity, which has been used to visualize cholinergic neurons and their processes in the central nervous system, is less successfully applied to the peripheral cholinergic system, especially in rats, without the use of specific antiserum against peripheral ChAT (41,54). The number of ChAT-positive neurons in the gastric myenteric plexus in acute cold-exposed rats observed in our previous study (73) did not match the data obtained using antiserum against peripheral ChAT (41).…”

Section: Discussionmentioning

confidence: 99%

Neuronal activation of brain vagal-regulatory pathways and upper gut enteric plexuses by insulin hypoglycemia

Yuan

Yang

2002

American Journal of Physiology-Endocrinology and Metabolism

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Yuan, Pu-Qing, and Hong Yang. Neuronal activation of brain vagal-regulatory pathways and upper gut enteric plexuses by insulin hypoglycemia. Am J Physiol Endocrinol Metab 283: E436-E448, 2002;10.1152/ajpendo.00538.2001.-Neuronal activation of brain vagal-regulatory nuclei and gastric/duodenal enteric plexuses in response to insulin (2 U/kg, 2 h) hypoglycemia was studied in rats. Insulin hypoglycemia significantly induced Fos expression in the paraventricular nucleus of the hypothalamus, locus coeruleus, dorsal motor nucleus of the vagus (DMN), and nucleus tractus solitarii (NTS), as well as in the gastric/duodenal myenteric/submucosal plexuses. A substantial number of insulin hypoglycemia-activated DMN and NTS neurons were choline acetyltransferase and tyrosine hydroxylase positive, respectively, whereas the activated enteric neurons included NADPH-and vasoactive intestinal peptide neurons. The numbers of Fos-positive cells in each above-named brain nucleus or in the gastric/duodenal myenteric plexus of insulin-treated rats were negatively correlated with serum glucose levels and significantly increased when glucose levels were lower than 80 mg/dl. Acute bilateral cervical vagotomy did not influence insulin hypoglycemia-induced Fos induction in the brain vagal-regulatory nuclei but completely and partially prevented this response in the gastric and duodenal enteric plexuses, respectively. These results revealed that brain-gut neurons regulating vagal outflow to the stomach/ duodenum are sensitively responsive to insulin hypoglycemia. dorsal motor nucleus of the vagus; nucleus tractus solitarii; glucose; vagus; stomach CONVERGING EVIDENCE SUGGESTS that hyper-or hypoglycemia affects gastrointestinal (GI) functions by influencing vagal-cholinergic outflow to the viscera. The involvement of upper GI tract organs in the hyperglycemia-induced delay of gastric emptying (5) corresponds to the distribution of the vagus in the GI tract (52). GI functions that are well established to be stimulated by vagal efferent activation, such as sham feeding-induced gastric acid secretion and pancreatic polypeptide release from the pancreas, were remarkably reduced during hyperglycemia (34). In contrast to hyperglycemia, insulin hypoglycemia is well established as a central vagal stimulus on upper GI functions (63,64,67). Visceral response to insulin hypoglycemia has been widely used to test vagus nerve integrity (67), especially used postoperatively to test the result of vagotomy (45). These findings established a role of the vagus nerve in mediating the regulation of GI functions by altered glucose metabolism. However, how the neurons in the brain vagal-regulatory nuclei and GI enteric plexuses respond to hypo-or hyperglycemia is still poorly understood.The medullary dorsal vagal complex (DVC) is composed of the dorsal motor nucleus of the vagus (DMN) and the nucleus tractus solitarii (NTS), which respectively contain somata of parasympathetic efferents that project to the GI tract (4, 48, 61) and neurons receiving vagal afferent i...

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“…Um dos principais neurotransmissores excitatórios do sistema nervoso entérico é a acetilcolina (OSINSKI e BASS, 1993;NAKAJIMA et al, 2000). A acetilcolina é sintetizada pela enzima acetiltransferase e sua degradação é efetuada por ação enzimática (DOOD e ROLE, 1991).…”

Section: Métodos Utilizados Para Marcação Neuronalunclassified

“…A acetilcolina é sintetizada pela enzima acetiltransferase e sua degradação é efetuada por ação enzimática (DOOD e ROLE, 1991). A acetilcolinesterase (AChE) é a enzima responsável pela quebra da acetilcolina após sua liberação na fenda sináptica (OSINSKI e BASS, 1993) podendo ser utilizada como um marcador de atividade colinérgica (GABELLA, 1994), visto que, para a marcação da acetilcolina, não existe um método histoquímico (NAKAJIMA et al, 2000).…”

Section: Métodos Utilizados Para Marcação Neuronalunclassified

Repercussões morfológicas da lesão térmica corporal nos componentes do plexo mioentérico do jejuno de ratos adultos.

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Immunohistochemical demonstration of choline acetyltransferase of a peripheral type (pChAT) in the enteric nervous system of rats

Cited by 72 publications

References 34 publications

Neonatal maternal separation of rat pups results in abnormal cholinergic regulation of epithelial permeability

Neonatal maternal separation of rat pups results in abnormal cholinergic regulation of epithelial permeability

Neuronal activation of brain vagal-regulatory pathways and upper gut enteric plexuses by insulin hypoglycemia

Repercussões morfológicas da lesão térmica corporal nos componentes do plexo mioentérico do jejuno de ratos adultos.

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